Type II Diabetes Mellitus and other diseases resulting from endothelial dysfunction, and their associated complications are a principal cause of disabilities and deaths of individuals in the world. For example, in recent years more than 700,000 deaths have occurred annually in the United States alone as a result of coronary artery disease, and many more patients have been hospitalized for unstable angina, acute myocardial infarction, and congestive heart failure, which occur in greater than 70% of patients with diabetes as the disease progresses. Additionally, diabetes is the most common cause of chronic renal insufficiency and renal failure in industrialized societies and a major cause of blindness and limb loss due to leg ischemia.
There has been significant and extensive research for effective long-term treatment for diabetes. However, present treatments for such disorders are partial treatments such as administration of insulin, and oral hypoglycemic agents. These treatments have serious shortcomings in long-term effectiveness. The use of these treatments does not resolve the spectrum of molecular and physiologic abnormalities attendant to the diabetes processes.
Diabetes is a medical condition associated with low enos activity, and high superoxide and other free radicals being generated in association with cellular hyperglycemia. These abnormalities result in alterations and defects in cellular matrix composition and cellular function in a variety of cell types including the pancreas, liver, kidneys, endothelium and cardiovascular system.
Currently available treatments have to date been only partially effective for favorable long-term results. None of these treatments have been designed to maintain, improve, or restores cellular function of the cell matrix of these cited organs and tissues by impacting the cell matrix and control of the generation of nitric oxide, superoxide, and other free radicals.
The focus of current treatment methods is to react to potentially immediate danger to one's life. These treatments and their shortcomings include;                Insulin injections: Shortcoming: hypoglycemia, inconvenience, and discomfort of administration.        Diet: Shortcoming: hard to follow.        Oral Medication: Metformin, Glucophage, Shortcoming: for severe hyperglycemia it is insufficient and does not treat the other dysmetabolic effects of the disease.        Kidney-Pancreas transplant: Shortcoming: Can't find donors.        
None of these treatment methods is directed towards the underlying disease processes, the molecular causes of the disease or disorders, the effects of the hyperglycemia on the basal molecular organization and properties of the cells, or towards restoring the structure and function of the blood vessels and other cell types to levels that reduce or eliminate the danger posed by diabetes. There is no treatment designed to reduce the level of free radical generation, of cell matrix re-organization, cell membrane composition, of clotting activity or preservation of vascular thromboresistance.
In view of the foregoing, there is a significant need for a pharmacological composition and method that is directed towards treating the underlying diabetes disease process, and towards preserving and restoring the structure and improving the functions of the various cell types involved with the diabetic processes and in particular the function-structure properties of the endothelium which lines the entire cardiovascular system and which is the interface of the blood with the vascular system and a major determinant of effective renal function.
It is an objective of the present invention to provide a treatment, which is directed to preventing and minimizing dysfunctional atomic and molecular interactions within the human cellular matrix or cellular environment, which lead to diabetes.
It is another objective of the present invention to provide a treatment that is directed to retarding adverse consequences of free radicals generated in human cellular matrix. It is also another objective of the present invention to stimulate an increased production of nitric oxide within human cellular matrix or cellular environment and to decrease production and effects of superoxide and other free radicals throughout the course of the disease.
It is yet another objective of the present invention treatment of cardiovascular diseases, in particular cell surface based thrombosis, without appreciably increasing blood anticoagulation activity in patients.